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FNH 250 > Energy Metabolism > Flashcards

Energy Metabolism Flashcards

1
Q

What are the 8 B-vitamins?

A
  1. Thiamin (B1)
  2. Riboflavin (B2)
  3. Niacin (B3)
  4. Folate (B9)
  5. B6
  6. B12
  7. Pantothenic Acid (B5)
  8. Biotin (B7)
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2
Q

Give a brief introduction of B-vitamins.

A
  • All water-soluble vitamins
  • Integral part of COENZYMES used in enzymatic reactions in the body (minerals act as cofactors)
  • Do not directly supply energy, but facilitate release of energy from macronutrients – CHO, PRO, FAT
  • Important for healthy blood and nervous systems
  • Food preparation methods that limit the loss of water-soluble B vitamins: steaming, grilling, microwaving (except for loss of vitamin B12)
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3
Q

What is the role of a coenzyme?

A

Coenzymes activate enzymes to catalyze reactions

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4
Q

What are the dietary forms of B-vitamins?

A
  • B-vitamins found in foods in coenzyme form
  • Digestive process frees the vitamin from its coenzyme form
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5
Q

Discuss the absorption, transportation, and storage of B-vitamins.

A

Absorption - Free vitamins absorbed

Transportation - To liver first, then travels in bloodstream to cells - Once vitamin is inside cells, coenzyme reformed

Storage - No long term storage of water-soluble vitamins

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6
Q

Discuss the fortification of refined grain products with B-vitamins.

A
  • B-vitamins added to 100 grams of refined grain products: flour, white flour, enriched flour or enriched white flour
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7
Q

Who is at risk for deficiency of B-vitamins?

A

Alcoholics

  • decreased intake, decreased absorption, alcohol damage to organs, increased metabolic use, low “stores”, increased excretion

Poor/elderly/malnourished/homeless

  • decreased intake of food in general, and nutrient-dense foods in particular, can increase­ risk of deficiency
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8
Q

Discuss the relationship between Thiamin, Riboflavin, Niacin.

A
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9
Q

What happens if you are deficient in thiamin?

A
  • neural damage
  • muscle wasting
  • edema
  • Beri-beri
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10
Q

What happens if you are deficient in riboflavin?

A
  • Ariboflavinosis
    • stomatitis
    • cheilosis
    • glossitis
    • dermatitis
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11
Q

What happens if you are deficient in niacin?

A
  • Pellagra “rough” skin
    • Dermatitis
    • Diarrhea
    • Dementia
    • Death
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12
Q

What are three rich sources of thiamin, riboflavin, and niacin?

A

Thiamin - acorn squash, pork chop, pita, broccoli

Riboflavin - broccoli, milk, fortified plant milk, beef liver, mushrooms

Niacin - Mushrooms, beef liver, peanut butter, whole wheat bread

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13
Q

Discuss the absorption & activation of folate.

A
  • folate is found in foods in polyglutamate form; digestion cleaves off all but one glutamate unit and adds a methyl group (methylated form) before absorption
  • water-soluble nutrient – travels in bloodstream, first to liver then to other cells
  • once inside cells, the methylated form of folate is inactive
  • vitamin B12 accepts the methyl group from folate and in the process both vitamins (i.e., unmethylated folate and methylated B12) become active coenzymes
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14
Q

What do the parietal cells in the stomach secrete?

A

Hydrochloric acid & intrinsic factor

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15
Q

Briefly introduce vitamin B12

A
  • Very large molecule with Cobalt centre (cobalamin)
  • Needed in very small amounts
  • Only natural source is from animal foods (microorganisms)
  • Efficiently recycled
  • Some storage in the liver
  • Unique absorption process
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16
Q

What are the roles of vitamin B6?

A
  • coenzyme forms Pyridoxal, Pyridoxine, and Pyridoxamine are all forms of vitamin B6 that can be converted to the most active co-enzyme form, Pyridoxal Phosphate (PLP)
  • PLP needed in over 100 enzyme systems involving macronutrient (mostly protein) metabolism

Generating Energy from the Macronutrients

i. needed to release glucose from glycogen stores
ii. needed for interconversions of amino acids that can feed into the Krebs Cycle

Reducing Homocysteine Levels in the Blood – reduces risk of heart attack

Transamination of Amino Acids

i. production of non-essential amino acids in body
ii. without B6, all amino acids would become essential

Synthesis of White Blood Cells (WBC) – helps fight infection

Synthesis of Hemoglobin in RBC –needed to transport oxygen to the cells to allow for the production of energy inside cells

Conversion of Tryptophan to Niacin

Synthesis of Glucose (gluconeogenesis), Neurotransmitters (e.g., Serotonin, Dopamine), Steroid Hormones and Bile Acids

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17
Q

What are folate’s roles?

A
  • coenzyme form called TetraHydroFolate acid (THF) needed for:

Generating Energy from the Macronutrients

  • needed for inter-conversion of amino acids and other compounds that feed into the Krebs Cycle

Reducing Homocysteine (HCys) Levels in the Blood

  • leads to a reduced risk of heart disease (e.g., heart attack and stroke)
  • elevated levels of blood HCys increases blood clotting and may damage lining of blood vessels to increase plaque formation

Synthesis of DNA

  • cells with a fast turnover are actively reproducing DNA and are most affected by folate status (e.g., embryonic development, red blood cells, intestinal cells, healing of burns)

Activating Vitamin B12 Inside Cells
- vitamin B12 is needed to activate THF by accepting a methyl group from the proactive form of THF

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18
Q

What are the roles of vitamin B12?

A
  • coenzyme forms – Methylcobalamin and Adenosylcobalamin – needed for:

Activating the Folate Coenzyme (THF) Inside Cells – to synthesize DNA

Reducing Homocysteine (HCys) Levels in the Blood

  • reduces risk of heart disease (e.g., heart attack and stroke)

Synthesis and Maintaining the Integrity of the Myelin Sheath

  • insulation around nerve fibres; prevention of nerve damage and paralysis
19
Q

What is transamination?

A

Synthesis of non-essential amino acids

20
Q

What are the symptoms of folate deficiency?

A
  • anemia, diarrhea, GI tract damage, inflammation of tongue, irritability, depression, problems with nerve function
21
Q

Who are at risk of folate deficiency?

A
  • women taking oral contraceptives may be at increased risk for folate deficiency
  • chronic users of antacids or aspirin, smokers, alcoholics
  • burn victims, any individual with GI tract damage (i.e., replacing intestinal cells)
22
Q

What are the consequences (not symptoms) of folate deficiency?

A

Macrocytic Anemia

  • red blood cell (RBC) synthesis occurs in the bone marrow, immature RBC cannot divide and mature

because they cannot make new DNA without adequate folate, but they can increase in size, so they are large but still immature cells = MACROCYTIC (big cell) ANEMIA
-these immature RBC cannot efficiently carry oxygen in the blood to the cells

  • observable symptoms of anemia (e.g., fatigue, weakness, paleness, shortness of breath, cool body temperature, intestinal upset)
  • anemia = lack of adequate oxygen carrying capacity in blood to meet body needs

Elevated Homocysteine (HCys) Levels in the Blood

-increased risk of heart disease

Neural Tube Defects Developing During Early Pregnancy

  • high need of folate for rapid cell division especially with multiple birth pregnancies
  • closure of neural tube (developing brain and central nervous system) occurs in first 28 days of pregnancy
  • many women are unaware of their pregnancy until after this critical time
  • improper neural tube closure may cause neural tube defects (spina bifida) or anencephaly (absence of brain) in babies born to mothers of poor folate status
23
Q

What populations are at risk of vitamin B12 deficiency?

A

elderly, vegans, non-absorbers of B12, infants exclusively breastfed by vegan mothers, people with damage to parietal cells in the stomach where intrinsic factor is produced

24
Q

What are the causes of vitamin B12 deficiency?

A

a. Lack of Dietary Intake of B12 (least likely cause for deficiency, except for vegans)

-because of extremely efficient recycling in the body, it can take many years of inadequate/no dietary intake of B12 before symptoms appear

  • *b. Absorption Problems**
  • deficiency symptoms appear much more rapidly when absorption is inhibited
  • inadequate stomach acid production (atrophic gastritis) – limited release of B12 from protein in food, therefore, cannot bind to IF – can contribute to deficiency -more often due to lack of adequate production of IF

-symptoms most often seen in people who are unable to absorb/reabsorb B12

25
Q

What are the consequences of vitamin B12 deficiency?

A

a. Patchy Myelin Sheath
- incomplete myelin sheath causing neurological damage, which can lead to paralysis

b. Macrocytic (Pernicious) Anemia – Secondary Folate Deficiency Inside Cells

26
Q

What is pernicious anemia?

A

PERNICIOUS ANEMIA = genetic disorder

  • caused by a defective gene that results in inadequate production of Intrinsic Factor, therefore, B12 absorption impaired
  • inability to absorb B12, not due to decreased dietary intake of B12
27
Q

What are the recommendations for B6, B12, and folate?

A
28
Q

What are food sources for B6, B12, and folate?

A

B6 - acorn squash, salmon, broccoli, blueberries

Folate - broccoli, asparagus, lentils

29
Q

Discuss supplementing B6 and folic acid.

A
30
Q

What are food sources of panthothenic acid and biotin?

A
31
Q

What are the roles of pantothenic acid?

A
  • -“pantos” = Greek for everywhere (widespread in the food supply)
  • coenzyme form called Coenzyme-A (CoA) is needed to synthesize:
    • acetyl-CoA which holds the central position in transforming energy from CHO, FAT and PRO through the Krebs cycle and electron transport chain to produce ATP
    • fatty acids, neurotransmitters, steroid hormones and hemoglobin
32
Q

What are the roles of biotin?

A
  • *intestinal synthesis by bacteria
  • coenzyme form called Biocytin and is needed for:
    • releasing energy from CHO
    • synthesis reactions – e.g., glucose, fatty acids, DNA
33
Q

Discuss deficiency of panthothenic acid and biotin.

A

Pantothenic acid: very rare, seen in alcoholics (symptoms: fatigue, headache, nausea, numbness, ‘burning foot’)

Biotin: very rare, seen in people on long-term antibiotics due to bacterial synthesis in the GI tract (symptoms: depression, lethargy, dermatitis, hair loss, loss of appetite.

34
Q

Discuss toxicity of panthothenic acid and biotin.

A

No cases of toxicity. No UL.

35
Q

Describe the roles, deficiency & toxicity risk of the vitamin-like compound choline.

A
  • serves as coenzyme, but is not essential in the diet
  • used to synthesize neurotransmitters and phospholipids
  • aids in reducing blood homocysteine levels
  • made in the liver from amino acids + folate + vitamin B12
  • found in many common foods: eggs, soybeans, milk, liver; often consumed as lecithin
  • deficiencies rare
  • increased intake may alter the fluidity of cell membranes which may lead to changes in function of the cell membranes, may lower blood pressure, cause diarrhea, and cause fishy body odour
36
Q

How does food storage/preparation affect nutrient losses?

A
37
Q

What are the roles of iodide?

A

Thyroid function - integral component of 2 thyroid hormones (triiodothyronine (T3) and thyroxine (T4)) that help control:

  • BMR
  • body temperature
  • nerve & muscle action
  • growth, reproduction
  • Selenium required (T4 > T3)

*80% of body iodide is found in thyroid gland.

38
Q

What are the roles of chromium?

A

Maintenance of blood glucose - Cr-containing protein binds to insuline receptors in cell membranes - this boosts receptor activity and cellular uptake of GLU from the blood to provide energy to cells.

0.4-2.5% of intake absorbed: organic acids (e.g., picolinate, vitamin C) increase absorption; antacids decrease absorption

39
Q

What are the roles of manganese?

A
  • Cofactor for many enzyme systems
    • arginase – urea synthesis
    • superoxide dismutase – antioxidant enzyme system in mitochondria
    • pyruvate carboxylase – used in CHO metabolism (pyruvate → oxaloacetate)
  • Cartilage production
40
Q

Discuss deficiency of iodide, chromium, and manganese.

A

Iodide - goiter, cretinism, weight gain

Chromium - may see higher blood glucose and insulin levels

Manganese - rare

41
Q

Discuss toxicity of iodide, chromium, and manganese.

A
42
Q

What are food sources of iodide, chromium and manganese?

A
43
Q

What are the roles, deficiency & toxicity risks & recommedations for sulphur?

A
44
Q

What are food sources of sulphur?

A

FNH 250 (11 decks)

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